An evolutionary approach to develop durable disease resistance to bacterial canker of cherry

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The resurgence of cherry production in the UK from 400 tonnes in the year 2000 to 3500 tonnes in 2014, achieved through the adoption of high-density plantings, has led to bacterial canker, which is caused by Pseudomonas syringae, becoming the main disease of cherry, for which there is no effective control. Our recent work has shown that bacterial canker is not caused by a single bacterial population but by three distinct groups of Pseudomonas, each having independently acquired the ability to cause disease on cherry and each manipulating the host in subtly different ways in order to subvert plant defences and survive in long term associations with the tree. This phenomenon is termed convergent evolution and is an interesting finding, as from it several fundamental scientific questions arise. In this proposal we seek to answer four questions, based upon recent research into this commercially important, yet understudied, pathogen. First, what is the basis of niche survival and persistence of P. syringae on cherry? We wish to understand if different complements of toxins, effectors (a special class of proteins secreted by the pathogen that are involved in suppressing plant immunity and promoting pathogen growth) and other gene clusters, implicated in manipulation of host defences, determine survivability in particular niches (in woody tissues for example) or at particular times of year, and whether these are different in our three Pseudomonas clades? Second, how is host specificity determined by effector content? Do conserved effectors, over-represented in convergently evolved Pseudomonas groups when compared to closely related non-cherry or plum pathogens, play an essential role in adaptation onto these hosts? This evolutionary approach, integrating information from many different strains of Pseudomonas is a novel way of utilising patterns of molecular evolution to provide insights into which pathogen genes are important targets for further study. Addressing these two questions will provide fundamental insights into how pathogens evolve onto their hosts and may provide new avenues to pursue when considering how to control these pathogens in the field. Third, which effectors control known resistance responses in cherry? This is a crucial question. Part of the plant immune system is controlled by specific classes of genes (broadly termed resistance or R genes) that have evolved to encode proteins that recognise pathogen attack, by monitoring for the presence or activity of effectors and then rapidly activating plant defence responses. Effectors are often referred to as the pathogen's Achilles heel, as they are both required for pathogenicity but leave the pathogen vulnerable to detection. Understanding which effectors are recognised in cherry material is important to predict the likely usefulness of particular plant resistances. For example, recognition of a rare effector at low frequencies in a pathogen population is less useful than an R gene that recognises a highly conserved effector, essential for pathogenicity. Our approach seeks to identify resistance genes that target effectors that are common to all strains of cherry infecting Pseudomonas, as well as other previously identified, but uncharacterised, resistances. Fourthly, what is the genetic architecture of resistance to P. syringae in cherry? By identifying the regions of the cherry genome that control resistance, using a technique called genetic mapping, molecular markers tagging R genes can be developed and used by the UK industry (plant breeders) in order to breed cherry cultivars resistant to all three groups of pathogenic Pseudomonas.Answering these questions provides plant breeders with the information that they require to develop resistant cultivars, improving yield, quality and the profitability of the industry and reducing waste in the supply chain.